|
Esophageal Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
Betel quid and tobacco chewing habit synergistically with p16 methylation elevated the risk for esophageal cancer development (adjusted odds ratio (OR) = 6.88, 95% confidence interval (CI) = 1.64-28.81, p = 0.003 for betel quid chewing and adjusted OR = 7.02, 95% CI = 1.87-26.38, p = 0.001 for tobacco chewing).
|
25361631 |
2015 |
|
Esophageal Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
SNHG7 can partly promote the development of esophageal cancer by regulating the expression of p15 and p16.
|
29771415 |
2018 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
This study investigated the immunohistochemical expression of retinoblastoma (RB) protein and p16 protein in 10 neuroendocrine carcinomas (NECs), in comparison to two mixed-type NECs; 28 squamous cell carcinomas (SCCs), and 12 carcinosarcomas (CSs) from patients with esophageal cancer.
|
30952735 |
2019 |
|
Esophageal Neoplasms
|
0.800 |
GeneticVariation
|
group |
BEFREE |
These findings suggest that loss or mutations of the p16 gene are involved in most esophageal cancers and that mutation of this gene plays a critical role in the development of esophageal cancer.
|
8093026 |
1994 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene.
|
28693288 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
Aberrant methylation of p16INK4a and deletion of p15INK4b are frequent events in human esophageal cancer in Linxian, China.
|
9934853 |
1999 |
|
Esophageal Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
The aim of this study is to offer a systematic review on the aberrant methylation of p16 gene in esophageal cancer.
|
24240582 |
2013 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
Our findings indicate that CDKN2A methylation has a vital role in EC tumorigenesis and could be a biomarker for early diagnosis of EC.
|
28637022 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
We report a highly frequent homozygous deletion of the p16/CDKN2 gene in the esophageal cancer cell line and a relatively high frequency of homozygous deletion in gastric cancer cell lines.
|
7614482 |
1995 |
|
Esophageal Neoplasms
|
0.800 |
GeneticVariation
|
group |
BEFREE |
p53 and p16/CDKN2 gene mutations in esophageal tumors from a high-incidence area in South Africa.
|
9808520 |
1998 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
The p53 expression was positive in 67.5% of tumor tissue, 20.0% of adjacent non-tumoral tissue and 1.8% of normal esophageal tissue. p16 was positive in 11.6% of esophageal cancer cases and 4.7% of adjacent non-tumoral tissue. p16 was undetectable among control group samples. p53 and p16 levels were not significantly associated with the HPV status.
|
28529620 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
GeneticVariation
|
group |
BEFREE |
Hypermethylation of p16 gene was not found in healthy controls. p53 Pro/Pro genotype was found to be a risk genotype in Northeast India compared with Arg/Pro and Arg/Arg. p53 variant/polymorphism was significantly associated with esophageal cancer risk in the study population under all three genetic models, namely, dominant model (Arg/Pro + Pro/Pro vs Arg/Arg odds ratio = 2.25, confidence interval = 1.19-4.26; p = 0.012), recessive model (Arg/Arg + Arg/Pro vs Pro/Pro odds ratio = 2.35, confidence interval = 1.24-4.44; p = 0.008), and homozygous model (Pro/Pro vs Arg/Arg odds ratio = 3.33, confidence interval = 1.54-7.20; p = 0.002).
|
28459370 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
Treatment of human esophageal cancer KYSE 510 cells with 5-50 microM of EGCG for 12-144 h caused a concentration- and time-dependent reversal of hypermethylation of p16(INK4a), retinoic acid receptor beta (RARbeta), O(6)-methylguanine methyltransferase (MGMT), and human mutL homologue 1 (hMLH1) genes as determined by the appearance of the unmethylation-specific bands in PCR.
|
14633667 |
2003 |
|
Esophageal Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
Associations of risk factors obesity and occupational airborne exposures with CDKN2A/p16 aberrant DNA methylation in esophageal cancer patients.
|
20459442 |
2010 |
|
Esophageal Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
HPV infection and p53 and p16 expression in esophageal cancer: are they prognostic factors?
|
29046713 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
A tissue microarray containing 86 specimens from esophageal cancer and 40 specimens from adjacent non-cancer tissue was constructed to survey the expression of p53, p16 and COX-2 by immunohistochemistry.
|
17650224 |
2007 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
Esophageal cancer is one primary human tumor in which MTS1 constitutes an apparent target of heterozygous or homozygous deletions occurring at chromosome 9p21.
|
7970734 |
1994 |
|
Esophageal Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
However, down-regulation of p16 and p21 occurred frequently in esophageal cancer, owing to aberrant gene promoter methylation.
|
16488074 |
2007 |
|
Esophageal Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
Low expression of (or IHC-negative) COX2, miR-200c, ERCC1 and TS, or high expression of (or IHC-positive) CDC25B and p16 are potential biomarkers for predicting the response of esophageal cancer patients treated with chemo(radio)therapy.
|
29113666 |
2017 |
|
Esophageal Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
The dual hits (concomitant loss) of pRb and p16INK4a expression suggest that these two components are not mutually exclusive, and can both be altered in a significant proportion of primary ESCCs serving as putative diagnostic markers for esophageal cancer.
|
11079730 |
2000 |
|
Lung Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
Moreover, the reverse correlation between p16INK4a immunostaining and p16INK4a promoter hypermethylation was also only observed in nonsmoking female lung tumors.
|
15455389 |
2005 |
|
Lung Neoplasms
|
0.800 |
Biomarker
|
group |
BEFREE |
Secondly, genetic resistance to lung tumor formation appears to segregate with one particular haplotype, which also is deleted preferentially in lung adenocarcinomas of Cdkn2a heterozygous mice.
|
10365910 |
1999 |
|
Lung Neoplasms
|
0.800 |
AlteredExpression
|
group |
BEFREE |
Western blot analysis showed that stromal cells of lung tumours were characterised by a statistically significantly lower expression level of the p16 protein as compared with that in normal lung stromal cells.
|
20407446 |
2010 |
|
Lung Neoplasms
|
0.800 |
PosttranslationalModification
|
group |
BEFREE |
In multivariate analysis, p16 hypermethylation was more prevalent in lung tumours from male than female patients (P = 0.018) and in squamous cell carcinomas than in adenocarcinomas (P = 0.025).
|
22217548 |
2012 |
|
Lung Neoplasms
|
0.800 |
GeneticVariation
|
group |
BEFREE |
The formation of lung tumors by these chemicals involved mutations in the K-ras cancer gene and loss of heterozygosity in the region of K-ras on distal chromosome 6, while alterations in p53 and p16 were implicated in brain tumorigenesis.
|
16860786 |
2007 |